Changes in the activities of antimicrobial, antitumor, and antioxidant properties of postbiotics (YCG) are related to changes in the composition of phenolic compounds. Antimicrobial activity was found to be highest in postbiotic (YCG-7) against P. aeruginosa, S. aureus, and E. faecalis with an MIC of 3.1 µg/mL. YCG-7 revealed the most cytotoxicity against LS-174T and PC-3 cell lines with an IC₅₀ of 5.78 and 6.56 µg/mL, respectively. YCG-7 was far more effective for scavenging free radicals in the NO^• and DPPH assays with a scavenging activity of 70.73% and 85.6%, respectively. YCG-7’s total phenolic acid content is up to eightfold higher compared with control. Escherichia coli Nissle 1917 retained high viable counts during refrigerated storage, particularly in YCG (>10⁸ cells g⁻¹) revealing a potential prebiotic activity of Cape gooseberry juice. EcN affected the phenolic profile of the YCG. Pyrogallol, p-coumaric acid, ellagic acid, 4-hydroxybenzoic acid, salicylic acid, gallic acid, vanillic acid, o-coumaric acid, caffeic acid, catechol, syringic acid, and rutin were the predominant phenolic compounds in YCG-7 or YCG-15. Chlorogenic, rosmarinic, cinnamic acid, naringin, and kaempferol were degraded by EcN in YCG-7 and YCG-15. The YCG had significantly higher sensory scores for appearance, smoothness, sourness, mouthfeel, and overall acceptance. These results provide the basis to target the functional benefits of YCG for further human health applications.

Fatty liver disease (FLD) is a growing public health problem worldwide. There is an urgent requirement for alternative and natural medicine to treat this disease. As phytochemicals, isoflavones have attracted considerable attention for the prevention of FLD. Numerous studies have revealed that isoflavones protect against FLD through various pathways which modulate fatty acid β-oxidation, lipid synthesis, and oxidative stress. Recently, the aldose reductase (AR)/polyol pathway has been reported to be involved in the development of FLD by modulating hepatic fructose production, peroxisome proliferator-activated receptor (PPAR)α activity, cytochrome P450 (CYP)2E1 expression, and gut bacterial endotoxin-induced cytokine release. It has been reported that some isoflavones are potent AR inhibitors. Here, we review the anti-FLD actions of isoflavones and the proposed mechanism whereby isoflavones protect against FLD, with regard to the AR/polyol pathway. We propose that isoflavones block the AR/polyol pathway and in turn reduce fructose production and subsequent fat accumulation in the liver in diabetic or high-glucose-diet mice. In addition, in rodents with alcoholic liver disease or nonalcoholic fatty liver disease/nonalcoholic steatohepatitis, inhibition of AR by isoflavones may improve PPARα-mediated fatty acid oxidation, reduce hepatic steatosis, and attenuate CYP2E1-mediated oxidative stress or AR/gut bacterial endotoxin-mediated cytokine overproduction, to alleviate progression of FLD.